A typical example of myolytic disease is muscular dystrophy. Muscular dystrophy is a general name for refractory muscular diseases where muscle suffers from necrosis and degeneration in a progressive manner whereupon muscle weakness is progressing. Among them, Duchenne's's muscular dystrophy (DMD) is a dystrophy having the highest frequency. In DMD, dystrophin is hardly produced, due to genetic abnormality of dystrophin. Since dystrophin constructs the skeleton of muscle cells, muscular cells in DMD are unable to keep their shape and necrosis easily happens. Cardiac and respiratory disorder caused by muscle weakness results in death.
With regard to a therapy for this disease, gene and transplantation therapies have been attempted but a basic remedy for the disease has not yet been developed. With regard to a drug therapy, a steroid pulse therapy with adrenocortical hormone (refer to Burrow K L, et al., Neurology, 41(5):661–6) and administration of antibiotics (gentamicin) (Barton Davis ER, et al., J. Clin. Invest., 104(4):367–368) have been applied. However, these symptomatic therapies are associated with severe side effects. Furthermore, the therapeutic effect lowers during long-term adminidtration. Especially in the case of DMD, a life-prolongation is expected only for about one year. Expression of H-PGDS increases in necrotic muscles of patients with DMD or multiple myolysis (Okinaga T, et al., Acta Neuropathol. (Berl). 2002 October; 104(4):377–84. Epub 2002 June). Therefore, it is likely that substances which regulate expression of H-PGDS and production and/or signal transduction of prostaglandin D2 are able to be effective therapeutic agents for such morbid states.